scholarly journals Factors that prevent the premature appearance of glucokinase in neonatal rat liver

1980 ◽  
Vol 186 (3) ◽  
pp. 817-826 ◽  
Author(s):  
M J O Wakelam ◽  
M B Allen ◽  
D G Walker
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Rat Liver ◽  
Neonatal Rat ◽  
Oral Glucose ◽  
Dibutyryl Cyclic Amp ◽  
Simultaneous Treatment ◽  
Physiological Factors ◽  
Glucose Administration

1. The physiological factors that prevent the precocious appearance of glucokinase activity in the 13-day-old rat that can be induced by oral glucose administration were explored. 2. Evidence is presented that the galactose component of milk sugar is inhibitory. In the absence of this inhibitory galactose, the amount of glucose necessary to effect appreciable induction is greater than that present in milk. 3. The induction is prevented both by administration of mannoheptulose, which inhibits insulin release, and by excess insulin; the amount of insulin available therefore seems to be critical. 4. The inhibition of induction by galactose does not appear to be via competition with glucose but by enhancing insulin release and thereby making this excessive. The relative amounts of glucose and insulin appear to be important in regulating glucokinase induction. 5. The precocious induction of glucokinase by glucose is inhibited by simultaneous treatment with approriate amounts of adrenaline, glucagon, dibutyryl cyclic AMP or isoprenaline but not by vasopressin or angiotensin II. 6. No single cause of glucokinase induction in neonatal rat liver can be recognized. The process is subject to regulation by many factors at a time subsequent to when competence to synthesize the enzyme has been established.

scholarly journals Hormonal regulation of glycogen metabolism in neonatal rat liver

1973 ◽  
Vol 134 (4) ◽  
pp. 985-993 ◽  
Author(s):  
Alan L. Schwartz ◽  
Theodore W. Rall
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Hormonal Regulation ◽  
Glycogen Metabolism ◽  
Hormonal Control ◽  
Neonatal Rat ◽  
Synthetase Activity ◽  
Dibutyryl Cyclic Amp ◽  
Glycogen Concentration ◽  
Glycogen Synthetase

1. The development of active and inactive phosphorylase was determined in rat liver during the perinatal period. No inactive form could be found in tissues from animals less than 19 days gestation or older than the fifth postnatal day. 2. The regulation of phosphorylase in organ cultures of foetal rat liver was examined. None of the agents examined [glucagon, insulin or dibutyryl cyclic AMP (6-N,2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate)] changed the amount of phosphorylase activity. 3. Glycogen concentration in these explants were nevertheless decreased more than twofold by 4h of incubation with glucagon or dibutyryl cyclic AMP. Incubation with insulin for 4h increased the glycogen content twofold. 4. Glycogen synthetase activity was examined in these explants. I-form activity (without glucose 6-phosphate) was found to decrease by a factor of two after 4h of incubation with dibutyryl cyclic AMP, whereas I+D activity (with glucose 6-phosphate) remained nearly constant. Incubation for 4h with insulin increased I-form activity threefold, with only a slight increase in I+D activity. 5. When explants were incubated with insulin followed by addition of dibutyryl cyclic AMP, the effects of insulin on glycogen concentration and glycogen synthetase activity were reversed. 6. These results indicate that the regulation of glycogen synthesis may be the major factor in the hormonal control of glycogen metabolism in neonatal rat liver.

Effect of epinephrine and dibutyryl cyclic AMP on Δ5-desaturation activity of rat liver microsomes

Lipids ◽  
1980 ◽  
Vol 15 (12) ◽  
pp. 1064-1066 ◽  
Author(s):  
I. N. T. de Gomez Dumm ◽  
M. J. T. de Alaniz ◽  
R. R. Brenner
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Dibutyryl Cyclic Amp ◽  
Desaturation Activity

scholarly journals Hepatic thiol and glutathione efflux under the influence of vasopressin, phenylephrine and adrenaline

1985 ◽  
Vol 226 (2) ◽  
pp. 545-549 ◽  
Author(s):  
H Sies ◽  
P Graf
Keyword(s):  
Plasma Membrane ◽  
Cyclic Amp ◽  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Peripheral Inflammation ◽  
Perfused Rat Liver ◽  
Dibutyryl Cyclic Amp ◽  
Hormone Dependence ◽  
Experimental Shock ◽  
Hormone Effects

Thiol and glutathione (GSH) efflux across the sinusoidal plasma membrane in isolated perfused rat liver was stimulated by addition of hormones such as vasopressin, phenylephrine and adrenaline, whereas glucagon or dibutyryl cyclic AMP were without effect. Phenylephrine and adrenaline effects were sensitive to prazosin and phentolamine, respectively. The increase in thiol efflux was largely accounted for by an increase in GSH efflux. Thiol efflux and the hormone effects were abolished in GSH-depleted liver. Biliary GSH efflux was diminished upon hormone addition. The newly discovered hormone-dependence of GSH release across the sinusoidal plasma membrane may explain the known loss of GSH during conditions of experimental shock (traumatic or endotoxin) and stress and peripheral inflammation.

scholarly journals Poly(adenosine diphosphate ribose) polymerase activity and nicotinamide adenine dinucleotide in differentiating cardiac muscle

1976 ◽  
Vol 154 (2) ◽  
pp. 387-393 ◽  
Author(s):  
W C. Claycomb
Keyword(s):  
Cyclic Amp ◽  
Dna Synthesis ◽  
Cardiac Muscle ◽  
Dna Polymerase ◽  
Specific Activity ◽  
Polymerase Activity ◽  
Neonatal Rat ◽  
Dibutyryl Cyclic Amp ◽  
Fresh Tissue ◽  
Dna Polymerase Α

Poly(ADP-ribose) polymerase activity in nuclei isolated from differentiating cardiac muscle of the rat has been characterized and its activity measured during development. Optimum enzyme activity is observed at pH 8.5. Poly(ADP-ribose) polymerase is inhibited by ATP, thymidine, nicotinamide, theophylline, 3-isobutyl-1-methylxanthine and caffeine and stimulated by actinomycin D. The activity measured under optimal assay conditions increases during differentiation of cardiac muscle and is inversely related to the rate of DNA synthesis and to the activities of DNA polymerase α and thymidine kinase. When DNA synthesis and the activity of DNA polymerase α are inhibited in cardiac muscle of the 1-day-old neonatal rat by dibutyryl cyclic AMP or isoproterenol, the specific activity of poly(ADP-ribose) polymerase measured in isolated nuclei is increased. The concentration of NAD+ in cardiac muscle increases during postnatal development. In the adult compared with the 1-day-old neonatal rat the concentration of NAD+ relative to fresh tissue weight, DNA or protein increased 1.7-fold, 5.2-fold or 1.4-fold respectively. The concentration of NAD+ in cardiac muscle of the 1-day-old neonatal rat can be increased by approx. 20% by dibutyryl cyclic AMP. These data suggest that NAD+ and poly(ADP-ribose) polymerase may be involved with the repression of DNA synthesis and cell proliferation in differentiating cardiac muscle.

scholarly journals Effect of phenylpyruvate on enzymes involved in fatty acid synthesis in rat brain

1973 ◽  
Vol 134 (2) ◽  
pp. 557-563 ◽  
Author(s):  
D. J. Deery ◽  
K. W. Taylor
Keyword(s):  
Cyclic Amp ◽  
Insulin Release ◽  
Acid Synthesis ◽  
Inhibitory Effect ◽  
Dibutyryl Cyclic Amp ◽  
Cell Content ◽  
Nad Synthesis ◽  
Arginine Hydrochloride ◽  
Rat Islets Of Langerhans

1. The effects of azaserine and nicotinamide, agents which inhibit and stimulate hepatic NAD synthesis respectively, on the content of NAD+ and NADH in isolated rat islets of Langerhans incubated in vitro were studied. The effects of these compounds on the rates of insulin release, from isolated islets incubated in vitro, in response to various secretagogues were also measured. 2. Preincubation of islets in the presence of azaserine (0.3mm) caused a marked depletion of the normal islet-cell content of both NAD+ and NADH and prevented the secretion of insulin in response to stimulatory concentrations of d-glucose, xylitol, d-xylulose, l-arginine hydrochloride and l-leucine. 3. Preincubation of islets in the presence of nicotinamide (2mm) increased the islet content of NAD+ and enhanced the rate of release of insulin in response to d-glucose. Also when nicotinamide was present the inhibitory effect of azaserine on insulin release and the azaserine-induced depletion of the islet content of NAD+ and NADH was prevented. 4. Preincubation with azaserine was without effect on the stimulation of insulin release caused by theophylline or dibutyryl cyclic AMP. 5. It is suggested that insulin release caused by sugars and amino acids is dependent on the maintenance of NAD concentrations, though this may not be the case for release due to theophylline and dibutyryl cyclic AMP.

scholarly journals Regulation of coenzyme A biosynthesis by glucagon and glucocorticoid in adult rat liver parenchymal cells

1980 ◽  
Vol 188 (1) ◽  
pp. 175-184 ◽  
Author(s):  
Colleen M. Smith ◽  
C. Richard Savage
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Maximum Effect ◽  
Maximal Effect ◽  
Dibutyryl Cyclic Amp ◽  
Liver Parenchymal ◽  
Adult Rat ◽  
Intracellular Mechanism ◽  
Inhibitor Of Protein Synthesis ◽  
Parenchymal Cells

We studied the effects of glucagon, dibutyryl cyclic AMP and dexamethasone on the rate of [14C]pantothenate conversion to CoA in adult rat liver parenchymal cells in primary culture. The presence of 30nm-glucagon increased the rate by about 1.5-fold relative to control cultures (range 1.4–2.3) and 2.4-fold relative to cultures containing 1–3m-i.u. of insulin/ml. The half-maximal effect was obtained at 3nm-glucagon. Dibutyryl cyclic AMP plus theophylline also enhanced the rate by about 1.5-fold. Dexamethasone acted synergistically with glucagon; glucagon at 0.3nm had no effect when added alone, but resulted in a 1.7-fold enhancement when added in the presence of dexamethasone (maximum effect at 50nm). The 1.4-fold enhancement caused by the addition of saturating glucagon concentrations was increased to a 3-fold overall enhancement by the addition of dexamethasone. However, dexamethasone added alone over the range 5nm to 5μm had no effect on the rate of [14C]pantothenate conversion to CoA. The stimulatory effect of dibutyryl cyclic AMP plus theophylline was also enhanced by the addition of dexamethasone. Changes in intracellular pantothenate concentration or radioactivity could not account for the stimulatory effects of glucagon, dibutyryl cyclic AMP or dexamethasone. Addition of 18μm-cycloheximide, an inhibitor of protein synthesis, decreased the rate of incorporation of [14C]pantothenate into CoA and the enhancement of this rate by glucagon and dibutyryl cyclic AMP plus theophylline in a reversible manner. These results demonstrate an influence of glucagon, dibutyryl cyclic AMP and glucocorticoids on the intracellular mechanism regulating total CoA concentrations in the liver.

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